BSNC 1000 Inflammation Exam with Correct Answers
Terms in this set (50)
Immunological defense intended to defend against cause of cell injury, eliminate
damaged tissue, and promote cell repair/generation
Inflammation
-nonspecific
-automatic
Immediate response to injury
Acute inflammation
-minutes to days
-eradicates harmful stimuli and initiates repair
-weeks to years
-tissue repeatedly damaged and repaired
Localized:
-granuloma (collection of fibroblasts, collagen, macrophages)
chronic inflammation
-e.g. TB
Systemic:
-results from disease or disease process
-e.g. rheumatoid arthritis
PRISH
Pain- caused by chemicals
Redness (erythema)
Signs and symptoms of inflammation
Immobility - if loss of function
Swelling
Heat
-Tissue injury/death
-Inflammatory mediators (NO, histamine) released locally by mast and injured tissue
List the main events of localized acute
cells
inflammation
-Vascular phase (vasodilation + permeability)
-Cellular phase (recruitment/margination/migration/chemotaxis + phagocytosis)
, Inflammatory mediators stimulate dilation and cell retraction.
1. Histamine binds to local endothelial cells -> vasodilation of small vessels near
Describe the vascular phase injury, causing more blood flow to the area
2. Endothelial cell retraction -> increased permeability
-> vascular contents (exudate) exit blood vessel into the injured area
Exudate contains Leukocytes, plasma proteins, inflammatory mediators
Serous (clear) exudate might be seen in a blister
Sanguineous exudate is indicative of open wound with ruptured blood vessel
An infection
Purulent (thick, brown) exudate is indicative
of
e.g. pus in abscess
Exudate fluid leaks through cell wall due to endothelial retraction, contains more
proteins
What is the difference between transudate
and exudate?
Transudate squeezes through because of fluid pressure imbalance (hydrostatic and
colloid osmotic)
1) Chemoattractants recruit WBCs (neutrophils + macrophages)
Margination:
-slower blood flow and vasodilation cause RBCs to become central and WBCs to
gather near periphery of lumen
-Surface markers called selectins (e.g. P selectin) "catch" the WBCs to slow them
down and keep them near endothelium
-WBCs "roll" along endothelium and then firmly adhere to endothelial wall via
integrins
-adherence pulls endothelial cells apart further
Transmigration: increased permeability allows WBCs to squeeze through gaps btwn
Describe the cellular stage
endothelial cells via diapedesis and move across cell wall into interstitial space
Chemotaxis: WBCs guided by pseudopodia to injured tissue/pathogen via gradient
of chemokines (e.g. cytokines like IL-8, C5 complement protein, etc.)
2) Phagocytosis of dead cells
a. Neutrophil/macrophage receptor recognizes and binds to target (b/c of
opsonization)
b. Endocytosis -> phagosome
c. Phagosome fuses with lysosome and is destroyed by lysosomal enzymes and
reactive oxygen species
Histamine
What are the 3 main inflammatory mediator
Cytokines
hormones?
Prostaglandin
What are the benefits of the inflammatory 1) restoring normal functioning cells after injury
response? 2) fibrous support when cells cannot be repaired
Which type of WBC is most prominent in neutrophils
acute inflammation?
What type of infection do neutrophils Bacterial
usually target?
Terms in this set (50)
Immunological defense intended to defend against cause of cell injury, eliminate
damaged tissue, and promote cell repair/generation
Inflammation
-nonspecific
-automatic
Immediate response to injury
Acute inflammation
-minutes to days
-eradicates harmful stimuli and initiates repair
-weeks to years
-tissue repeatedly damaged and repaired
Localized:
-granuloma (collection of fibroblasts, collagen, macrophages)
chronic inflammation
-e.g. TB
Systemic:
-results from disease or disease process
-e.g. rheumatoid arthritis
PRISH
Pain- caused by chemicals
Redness (erythema)
Signs and symptoms of inflammation
Immobility - if loss of function
Swelling
Heat
-Tissue injury/death
-Inflammatory mediators (NO, histamine) released locally by mast and injured tissue
List the main events of localized acute
cells
inflammation
-Vascular phase (vasodilation + permeability)
-Cellular phase (recruitment/margination/migration/chemotaxis + phagocytosis)
, Inflammatory mediators stimulate dilation and cell retraction.
1. Histamine binds to local endothelial cells -> vasodilation of small vessels near
Describe the vascular phase injury, causing more blood flow to the area
2. Endothelial cell retraction -> increased permeability
-> vascular contents (exudate) exit blood vessel into the injured area
Exudate contains Leukocytes, plasma proteins, inflammatory mediators
Serous (clear) exudate might be seen in a blister
Sanguineous exudate is indicative of open wound with ruptured blood vessel
An infection
Purulent (thick, brown) exudate is indicative
of
e.g. pus in abscess
Exudate fluid leaks through cell wall due to endothelial retraction, contains more
proteins
What is the difference between transudate
and exudate?
Transudate squeezes through because of fluid pressure imbalance (hydrostatic and
colloid osmotic)
1) Chemoattractants recruit WBCs (neutrophils + macrophages)
Margination:
-slower blood flow and vasodilation cause RBCs to become central and WBCs to
gather near periphery of lumen
-Surface markers called selectins (e.g. P selectin) "catch" the WBCs to slow them
down and keep them near endothelium
-WBCs "roll" along endothelium and then firmly adhere to endothelial wall via
integrins
-adherence pulls endothelial cells apart further
Transmigration: increased permeability allows WBCs to squeeze through gaps btwn
Describe the cellular stage
endothelial cells via diapedesis and move across cell wall into interstitial space
Chemotaxis: WBCs guided by pseudopodia to injured tissue/pathogen via gradient
of chemokines (e.g. cytokines like IL-8, C5 complement protein, etc.)
2) Phagocytosis of dead cells
a. Neutrophil/macrophage receptor recognizes and binds to target (b/c of
opsonization)
b. Endocytosis -> phagosome
c. Phagosome fuses with lysosome and is destroyed by lysosomal enzymes and
reactive oxygen species
Histamine
What are the 3 main inflammatory mediator
Cytokines
hormones?
Prostaglandin
What are the benefits of the inflammatory 1) restoring normal functioning cells after injury
response? 2) fibrous support when cells cannot be repaired
Which type of WBC is most prominent in neutrophils
acute inflammation?
What type of infection do neutrophils Bacterial
usually target?
